SCA1-like Disease in Mice Expressing Wild-Type Ataxin-1 with a Serine to Aspartic Acid Replacement at Residue 776
- 1 September 2010
- Vol. 67 (6), 929-935
- https://doi.org/10.1016/j.neuron.2010.08.022
Abstract
No abstract availableKeywords
This publication has 30 references indexed in Scilit:
- Serines 13 and 16 Are Critical Determinants of Full-Length Human Mutant Huntingtin Induced Disease Pathogenesis in HD MiceNeuron, 2009
- Full-Length Human Mutant Huntingtin with a Stable Polyglutamine Repeat Can Elicit Progressive and Selective Neuropathogenesis in BACHD MiceJournal of Neuroscience, 2008
- RNA toxicity is a component of ataxin-3 degeneration in DrosophilaNature, 2008
- Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1Nature, 2008
- RORα-Mediated Purkinje Cell Development Determines Disease Severity in Adult SCA1 MiceCell, 2006
- Wild-type microglia extend survival in PU.1 knockout mice with familial amyotrophic lateral sclerosisProceedings of the National Academy of Sciences, 2006
- The AXH Domain of Ataxin-1 Mediates Neurodegeneration through Its Interaction with Gfi-1/Senseless ProteinsCell, 2005
- Testosterone Reduction Prevents Phenotypic Expression in a Transgenic Mouse Model of Spinal and Bulbar Muscular AtrophyNeuron, 2002
- Aggregation of Huntingtin in Neuronal Intranuclear Inclusions and Dystrophic Neurites in BrainScience, 1997
- Expression analysis of the ataxin–1 protein in tissues from normal and spinocerebellar ataxia type 1 individualsNature Genetics, 1995